Myopia develops in macaque monkeys when their lids are surgically fused at birth and kept closed for one year. This experimental refractive error has many features in common with human myopia: It is caused by progressive axial elongation of the eye, is often accompanied by fundus changes, and can only be induced before eye growth has been completed. Myopia does not develop in animals raised in the dark; thus, it is triggered by an alteration of the visual input and is presumably mediated by the nervous system. In Macaca arctoides, atropine administration prevents abnormal eye elongation, and this suggests that lid-fusion myopia is caused by excessive accommodation. In M. mulatta, atropine is ineffective; furthermore, myopia develops when lids are sutured after interruption of the optic pathways. Thus, in this species accommodation can be ruled out as a determinant of eye elongation, and other neural mechanisms may be responsible for the refractive error. Our experiments suggest that the refractive state is largely programmed on a genetic basis, but that an abnormal visual experience can disrupt the process of postnatal eye growth and induce axial myopia.